Polycystic ovary syndrome is a common endocrine disorder characterized by hyperandrogenemia and menstrual disorders. Patients not only have a high incidence of insulin resistance and metabolic syndrome, but also a high incidence of sleep disorders, especially obstructive sleep apnea. Obesity, hyperandrogenemia, insulin resistance,and other factors are responsible for the high prevalence of sleep apnea in women with polycystic ovary syndrome.

Objective To study the effect of different fraction interval with same total radiation dose on tumor growth delay and survival in C57BL mice implanted with lewis lung cancer,and to determine whether prolonged fraction interval will decrease the tumor response to radiation. Methods Forty-eight mice were implanted with lewis lung cancer in the back legs.When the diameter of transplanted tumor reached 0.8 to 1 cm,the mice were randomized into 6 groups:normal control group,single fraction of 18 Gy group,18 Gy in 2 fractions of 9 Gy at 30 min interval group,18 Gy in 7 fractions of 2.57 Gy at 5 min inter val group,18 Gy in 2 fractions of 9 Gy at 60 min interval group and 18 Gy in 7 fractions of 2.57 Gy at 10 rain interval group.The maximal and minimal diameters of the tumor were measured and record every other day to study the tumor growth tendency,the tumor growth delay and the mice survival time. Results The tumor growth delay of groups at prolonged fraction interval was shorter than the group with single fraction of 18 Gy (P < 0.05).The tumor growth delay of groups at fraction interval of 30 rain was longer than that of groups at interval of 60 rain (P < 0.05).There was no significant difference of the tumor growth delay be tween the groups with same delivery time (P >0.05).The mice survival time of the groups with prolonged fraction interval was shortened when omparing to the group with single fraction of 18 Gy.While the difference was not significant between the groups at fraction interval of 30 min and 60 min. Conclusions The pro longed fraction interval but same total radiation dose shortens the tumor growth delay and survival time in the mice implanted with Lewis lung cancer.The longer fraction interval impairs the tumor control more signifi candy.However the difference of the effect on mice survival time is not significant between the groups at fraction interval of 30 min and 60 min.

Objective:To study the effect of ischemic postconditioning(I-postC)on the lung injury following ischemia-reperfusion(I/R)of skeletal muscle in the hind limbs of rats.Methods:The rat model of hind limbs I/R injury was established by subrenal abdominal aorta cross-clamping for 4 hours.Forty-eight rats were divided into 3 groups:I/R group,IPC and I-postC group.Each group received 4 hours of ischemia and then 12 or 24 hours of reperfusion respectively.The tissue morphology,wet-to-dry weight(W/D)ratio,malondialdehyde(MDA)and myeloperoxidase(MPO) of lung tissue were compared.The expression of ICAM-1 mRNA in lung was also studied by RT-PCR or in situ hybridization.The protein product was detected by Western blot.Results:In IPC and I-postC groups,all parameters decreased significantly compared with I/R ischemia group(P

Objective By observing the changes in NGF and its receptor P75 in liver of CCl4-induced toxic rats and to evaluate the role of NGF in the mechanism of hepatic fibrosis.Methods The expressions of NGF mRNA and its receptor P75 were detecteded by both hemi-quantitative RT-PCR and Western blot analysis.Results The expressions of NGF mRNA and its receptor P75 in liver of CCl4-induced toxic rats at 24th hour group were higher than that in control group(P

As one of the serious complications of diabetes, diabetic retinopathy( DR) has become a main eye disease which causes blindness. The occurrence and development of DR is related to many factors. The pathogenesis is complicated, and the mechanism has not been clear. Early data suggest that the occurrence and development of DR has relations with many factors such as blood sugar level, diabetes duration and the environment. Among the factors, mitochondrial dysfunction and oxidative stress is the important mechanisms of DR and has become research focus in recent years. Consequences of mitochondrial dysfunction within cells include elevation of the rate of reactive oxygen species( ROS) production due to damage of electron transport chain proteins, mitochondrial DNA ( mtDNA ) damage, and loss of metabolic capacity. Clear understanding on the mechanism of mitochondrial functional change under high sugar level and oxidative stress response in the occurrence and development of DR is of great significance on prevention and cure of DR. ln this article, the development of mitochondrial metabolism and oxidative stress of DR is reviewed.

Objective To determine effects of activating protein kinase C (PKC) on ventricular action potential duration restitution (APDR) and Burst stimulus induced arrhythmia in Langendorff-perfused rabbit hearts.Methods Male rabbits were equally divided into three groups randomly: control group (Tyrode's solution perfusion),PKC agonist phorbol-12-myristate-13- acetate (PMA,100 nmol/L) group and PKC inhibitor bisindolylmaleimide (BIM,500 nmol/L) group.Thirty minutes after perfusion,the monophasic action potential (MAP) and effective refractory period (ERP) were determined in right basal ventricle (RB),right apex ( RA ),left basal ventricle (LB) and left apex (LA) of all the animals,and APDR curve was drawn.Burst stimulus method was used to induce ventricular arrhythmia in perfused rabbit hearts; Real-time PCR was used to detect the mRNA expression of PKC in four different areas of ventricle.Results Compared with the control group,the ERP,90％ of monophasic action potential duration ( MAPD90 ) and ERP/MAPD90 were significantly shortened ( all P ＜ 0.01 ),the max slopes ( Smax ) of APDR curve were significantly steeper (RB:1.22 ±0.23 vs.0.65 ± 0.19 ; RA:2.99 ± 0.29 vs.1.02 ± 0.18 ;LB:1.84 ±0.21 vs.0.85 ±0.12; LA:4.02 ±0.32 vs.1.12 ±0.23,all P ＜0.01 ) and the incidences of ventricular arrhythmia were significantly increased in the PMA group.All parameters were similar between the BIM group and the control group (all P ＞ 0.05).Conclusion Activating PKC could enhance the max slopes of APDR curve at various ventricular areas and subsequently increase arrhythmia susceptibility in Langendorff-perfused rabbit hearts.

The deubiquitinating enzyme ubiquitin specific peptidase 15 (USP15) is regarded as a regulator of TGFβ signaling pathway. This process depends on Smad7, the inhibitory factor of the TGFβ signal, and type I TGFβ receptor (TβR-I), one of the receptors of TGFβ. The expression level of USP15 seems to play vital roles in the pathogenesis of many neoplasms, but so far there has been no report about USP15 in psoriasis. In this study, immunohistochemical staining of USP15, TβR-I and Smad7 was performed in 30 paraffin-embedded psoriasis specimens and 10 normal specimens to investigate the expression of USP15, TβR-I and Smad7 in psoriasis and to explore the relevance among them. And USP15 small interfering RNA (USP15 siRNA) was used to transfect Hacat cells to detect the mRNA expression of TβR-I and Smad7. Of 30 cases of psoriasis in active stage, 28, 24 and 26 cases were positive for USP15, TβR-I and Smad7 staining, respectively. The positive rates of USP15 and Smad7 were significantly higher in psoriasis specimens than in normal skin specimens (44.1%±26.0% vs. 6.1%±6.6%, 47.2%±27.1% vs. 6.6%±7.1%), and positive rate of TβR-I (20.3%±22.2%) in psoriasis was lower than that in normal skin specimens (46.7%±18.2%). There was a significant positive correlation between USP15 and Smad7 expression, and significant negative correlations between USP15 and TβR-expression, an I d between TβR- and Smad7 expression I in psoriasis. After transfection of USP15 siRNA in Hacat cells, the expression of TβR-mRNA was up I -regulated and that of Smad7 was down-regulated. It is concluded that USP15 may play a role in the pathogenesis of psoriasis through regulating the TβR-I/Smad7 pathway and there may be other cell signaling pathways interacting with USP15 to take part in the development of psoriasis.

OBJECTIVETo investigate effects of the variation of immune function in high humidity environment in different time, and lay a foundation for further study of the related mechanism.

METHODThirty SD rats were divided into 3 groups (n = 10): 20 day group, 40 day group in 90% relative humidity chamber and control group in normal relative humidity. Peripheral blood and spleens were collected to detect the levels of T lymphocyte subsets by Flow Cytometery.

RESULTSIn peripheral blood of the 20 day group rats, the CD3+ %, CD4+ %, CD8+ % and CD4+/CD8+ were 52.91 +/- 6.27, 37.80 +/- 4.11, 14.85 +/- 3.73 and 2.72 +/- 0.82 separately. Expect CD3+ %, they all had significant differences (P < 0.05). In addition, the data of the 40 day group rats showed no diversity in statistics. In spleen, CD8+ % of the 20 day group rats was 6.23 +/- 2.87 with significant differences (P < 0.05) and IgG, IgA and IgM did not change a lot in blood serum of the high humidity groups except C3 of the 20 days group (P < 0.05).

CONCLUSIONIn high humidity environment, the immune function of the rats increased in the initial stage. As time went on, the immune function gradually went to normal level through the self adjustment.

Objective To analyze the clinical features and gene mutation in mthylmalonic acidemia (MMA) accompanied by homocysteinemia (cblC), and review the relevant literatures. Methods The clinical features of 3 cases of MMA diagnosed by gene detection were retrospectively analyzed, and meanwhile the pertinent literatures of pathogenesis of MMA, especially combined with late-onset cblC and its gene detection, were reviewed. Results Patient 1 (26 days old) suffered from intermittent convulsions for 3 days, with isosuccinic acid 175.8 μmol/L, C3/C2 rate 1.363, homocysteine >?65 μmol/L and abnormal EEG. MMACHC gene detection found an exon deficiency (delEXON1), which has not been reported. Patient 2 ( 12 year old) was hospitalized for limb shaking, hyperspasmia and vomiting. His isosuccinic acid level was 334.3 μmol/L, C3/?C2 rate was 0.37, homocysteine >?65 μmol/L, and had abnormal EEG. MMACHC gene detection found the mutations of c.482G?>?A and c.609G?>?A. Patient 3 was hospitalized for intermittent convulsions for 20 days, whose isosuccinic acid, C3/?C2 rate, and homocysteine were increased. MMACHC gene detection found the mutations of c.394C?>?T and c.540del8 and c.540del8 had not been reported. Review of literatures discovered that MMA was combined with epileptic seizure in some patents, which further validate that the mutation in MMACHC gene c.482G?>?A may be related to the late-onset of cblC. Conclusions Gene detection contributes to the diagnosis of MMA; the mutation of MMACHC gene c.482G>A may be related to the late-onset of cblC; delEXON1 and c.540del8 are new mutations which have not been reported.

Aim: To investigate the pathological changes in NTBC[2-(2-nitro-4-trifluoro-methyl-benzoyl) -1,3 cy-clohexanedione]-induced hepatic injury in mice and in the repopulation of adult hepatocytes in Fah~(-/-) mouse. Methods: Autogenous hepatic injuries in Fah~(-/-) mice were induced by the treatment of NTBC. Injection of hepatocytes obtained from wild-type mice to spleen were transplanted into the Fah~(-/-) mice. Then, changes to body weight and the likelihood of the transplanted Fah~(-/-) mice, and hepatic immunohistochemistry were ob-served. In addition, pathological changes to liver damage induced by NTBC treatment were analyzed under HE-staining microscopy and electron microscopy. Results: The surviving Fah~(-/-) mice subjected to hepatocyte trans-plantation were found to be healthy and in stable body weight. liver repopulation reached to 90% in the 8th week. Repopulating hepatocytes caused no alteration to histological structure of the recipient liver, and subacute hepatic injury occurred in the Fah~(-/-) mice after NTBC treatment. Electronic microscopy observations indicated that necrosis in the hepatocytes occurred at early stage and that apoptosis gradually appeared. It was also shown both necrosis and apoptosis co-existed in the same samples of interest at the following stages of the induced liver injury. Conclusion: Transplanted hepatocytes proliferated in Fah~(-/-) mice allow 90% of the hepatocytic repopula- tion. Repopulation renders normal hepatic function and structure in the recipient Fah~(-/-) mice, as a model of liver repopulation, could be applicable in study of stem cell derived hepatic cells in transplantation assay.